[Chemiluminescence on hypoxic brain--the 1st report: relation between free radical reaction and energy metabolism]

To explore the possibility that cerebral ischemia or cerebral hypoxia may initiate a series of free radical reactions of brain tissue lipid constituents, we measured sequential change of chemiluminescence and energy metabolites during brain hypoxia in rat. The hypoxic brain was induced by arterial hypoxemia (PaO2 17-22 mmHg) with normocapnia (PaCO2 28-38 mmHg) and normotension (MABP 100-140 mmHg). 4% O2-96% N2 mixed gas was used as the replacement for obtaining lowered PaO2. We made another attempt to analyze chemiluminescence spectra on purpose of luminous mechanism investigation. No peroxidation occurred in prehypoxic state since there were no photon counts, however, chemiluminescence began to rise up in hypoxic state and remained high value in posthypoxic early state. Namely in hypoxic state, 3-min period showed 231 counts/10 sec X g and 5-min period showed 154 counts/10 sec X g. In posthypoxic state, 5-min period showed 217 counts/10 sec X g and 30-min period showed a similar decrease as prehypoxic state. The chemiluminescence spectroanalysis showed five peaks at 480 nm, 520-530 nm, 570 nm, 620-640 nm, 700 nm in wavelength. As to sequential changes of energy metabolism, hypoxia caused marked brain lactic acidosis, increase in ADP, pyruvate and a fall in glucose. However, all metabolites recovered at 30-min period in posthypoxic state, which suggests this was reversible brain hypoxia. A transition of chemiluminescence and energy metabolites suggests the occurrence of free radical reaction in hypoxic and posthypoxic brain. The spectroanalysis reveals the luminous mechanism as follows 1 delta g # 1 delta g----2(3)O(2) + h nu.